MINI REVIEW
published: 10 September 2018
Edited by:
Frank Ronald De Gruijl,
Leiden University Medical Center,
Netherlands
Reviewed by:
Vijaykumar Patra,
Medizinische Universität Graz, Austria
Sally Helen Ibbotson,
University of Dundee, United Kingdom
*Correspondence:
Serena Lembo
slembo@unisa.it
Specialty section:
This article was submitted to
Dermatology,
a section of the journal
Frontiers in Medicine
Received: 29 May 2018
Accepted: 22 August 2018
Published: 10 September 2018
Citation:
Lembo S and Raimondo A (2018)
Polymorphic Light Eruption: What’s
New in Pathogenesis and
Management. Front. Med. 5:252.
doi: 10.3389/fmed.2018.00252
Frontiers in Medicine | www.frontiersin.org
doi: 10.3389/fmed.2018.00252
Polymorphic Light Eruption: What’s
New in Pathogenesis and
Management
Serena Lembo 1* and Annunziata Raimondo 2
1
Department of Medicine, Surgery and Dentistry, “Scuola Medica Salernitana”, University of Salerno, Salerno, Italy,
2
Department of Clinical Medicine and Surgery, University of Naples, Federico II, Naples, Italy
Polymorphic light eruption is the commonest photosensitive disorder, characterized by
an intermittent eruption of non-scarring erythematous papules, vesicles or plaques that
develop within hours of ultraviolet radiation exposure of patient skin. Together with the
lesions, a terrible itch starts and increases with the spreading of the disease, sometimes
aggravated by a sort of burning sensation. Clinical picture and symptoms can improve
during the rest of the summer with further solar exposures. In the last years many
advances have been performed in the knowledge of its pathogenesis and some news
have been proposed as preventive, as well as therapeutic options. All this has been
discussed in the current mini review.
Keywords: polymorphic light eruption, photosensitive disorders, phototherapy, apoptosis, delayed type
hypersensitivity reaction
INTRODUCTION
During winter, sometimes dermatologists receive asymptomatic patients, with no specific lesions
other than, perhaps, some post-inflammatory discoloration, but with a desperate need for help.
They start to tell the story of a number of papules or vesicles appearing on their skin after the
first intense sun exposure of the year. Together with the lesions, a terrible itch starts and increases
with the spreading of the disease, following the next sun exposure, sometimes aggravated by a sort
of burning sensation. Nevertheless, this people are model sun seekers and continue to enjoy the
sunshine throughout the summer, waiting for the papules to gradually fade and disappear. The
main questions are: how can I prevent this? Why I’m getting this problem since “5” years now, but
I never had it before?
We are most probably dealing with polymorphic light eruption (PLE) and, following the
requests of our patients, medical research has mainly been focused on prevention strategies become
nowadays quite satisfactory. On the other side, the second and certainly less explored question
remains unclear, unless multiple pieces have been added to this rather complicate puzzle. Aim of
this brief review is to resume the most recent advances in PLE possible mechanisms and the most
used protocols for prevention or treatment.
1 September 2018 | Volume 5 | Article 252
Lembo and Raimondo Polymorphic Light Eruption: News Overview

PATHOPHISIOLOGY OF POLYMORPHIC
LIGHT ERUPTION: WHAT’S NEW?
PLE is the commonest photosensitive disorder, characterized by
an intermittent eruption of non-scarring pruritic erythematous
papules, vesicles or plaques (Figure 1) that develop within
hours of ultraviolet radiation (UVR) exposure of patient skin.
The disease is dependent on genetic susceptibility, as well
as environmental component, such as type of exposure. PLE
appears to cluster in families: it has been estimated that the
prevalence of PLE was 21 and 18% in monozygotic and dizygotic
twins, respectively (1). Moreover, a positive family history of
PLE in first-degree relatives was present in 12% of affected twin
pairs respect to 4% of unaffected twin pairs (p < 0.0001). The
probandwise concordance in monozygotic was superior than in
dizygotic twin pairs (0.72 vs. 0.30, respectively), demonstrating
a strong genetic effect (1). Many genes of potential interest in
FIGURE 1 | Clinical picture of polymorphic light eruption in a young woman.
the pathogenesis of PLE have been investigated with generally
unrewarding results. Using segregation analysis, it has been
estimated that 72% of the UK population carry a low penetrance
thereafter transformed in auto-reactive T cells (6, 7). This
PLE susceptibility allele (2).
partial failure of the apoptosis contributes, together with the
inadequate immunosuppression after UV exposure, to the
The Failure of Apoptosis: the Possible antigen recognition and presentation, leading to the clinical
Photo-Induced Neo Antigens manifestation typical of PLE patients (8). Indeed, the failure of
In a recent genome-wide expression analysis, only 16 genes normal UVR-induced immunosuppression has been proved as
were differentially expressed between PLE and healthy controls the main immunological abnormality in PLE, explained, initially,
after UV irradiation respect to control (3). Of these genes, 14 by the permanence of Langerhans cells (LCs) in the epidermis.
showed lower expression in PLE patients, whereas two resulted This over-activation of the immune system, which escapes to the
over-expressed. Among the 14 genes with lower expression functional UV-induced tolerance, is probably responsible for the
in PLE are: complement 1s subunit (C1s), scavenger receptor reduced skin cancer prevalence in PLE patients (9). On the other
B1 (SCARB1) fibronectin (FN1), immunoglobulin superfamily hand, the same mechanism is guilty for the failure of allergic
member 3 (IGSF3), caspase-1 (CASP1) and paraoxonase 2 contact dermatitis (ACD) suppression, after UVR exposure (10).
(PON2), all genes associated with apoptotic cell clearance. It
has been supposed that protein modification during apoptotic
Inflammatory Pathway: Delayed-Type
cell clearance could lead to potential auto-antigen formation (4).
Then, the reduced expression in PLE patients of genes connected Hypersensitivity Reaction
to this process might represent a possible auto-antigen source, The immunological mechanisms involved in PLE, with mediators
as well as a crucial phase in the initiation of the autoimmune from the innate and adaptive immune system, are very similar,
process that promotes the disease (3). In accordance to these either from the histological or the biochemical point of view,
findings, Kuhn et al. showed accumulation of apoptotic cells in to the ACD ones. In effect, in the early seventies, Epstein
PLE patients irradiated either with 1.5 Minimal Erythema Dose first indicated PLE as a delayed-type hypersensitivity reaction
(MED) of UVB, or 60–100 J/cm2 of UVA1, compared to controls (DTHR) to undefined UVR-induced cutaneous antigen (11).
(5). Recently, to reinforce this concept, some of the inflammatory
mediators involved in ACD have been demonstrated also in
Immunity: Tolerance’s Failure PLE. For example, IL-1 family (12, 13), a growing group of
Auto-antigens deriving from the inefficient clearance of cytokines that play several roles in immune regulation and
apoptotic cells, are probably taken up by dendritic cells inflammation (14), involved also in ACD pathogenesis (12, 15),
(DCs) and presented to naive T-cells (cytotoxic and helper) has been explored also in PLE (16). IL-36α and IL-36γ, the
pro-inflammatory members of IL-1 family were increased in
Abbreviations: IL, Interleukin; PLE, Polymorphic light eruption; ACD, Allergic
PLE respect to controls, as for ACD samples, but IL-36γ was
contact dermatitis; DTHR, Delayed type hypersensitivity reaction; UVR, much enhanced in PLE than in ACD (16). Acting through
Ultraviolet radiation; C1s, Complement 1s subunit; SCARB1, Scavenger receptor the common receptor composed of IL-36R and IL-1R/AcP
B1; FN1, Fibronectin; IGSF3, Immunoglobulin superfamily member 3; CASP1, (IL-1RL2), IL-36α, IL-36β, and IL-36γ activate NF-κB and
Caspase-1; PON2, Paraoxonase 2; MED, Minimal Erythema Dose; DCs, Dendritic MAPKs, promoting inflammatory reactions. The increase of IL-
cells; LCs, Langerhans cells; TLR, Toll like receptor; AMPs, Antimicrobial
peptides; SPF, Sun protection factor; PUVA, Psoralen and UVA therapy; NB-UVB,
36s in skin and peripheral blood of PLE patients indicates the
Narrowband; BB-UVB, Broadband UVB; MPD, Minimum phototoxic dose; Tregs, activation of local and systemic immune response, as found in
Regulatory T cells; PL, Polypodiumleucotomos. multiple inflammatory skin conditions (15, 17, 18). Probably,

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Lembo and Raimondo
the link between IL-36s and UVR exposure is represented
by the paracrine pro-inflammatory signal of toll like receptor
(TLR)-3 activation, due to the release of RNA by necrotic
keratinocytes (19). Indeed, the failure of apoptotic clearance in
PLE, with abundance of cellular debris, could be responsible for
an amplification of this “alert signal.”
Moreover, IL-36s could contribute to amplify the innate
immune signal and the consequent inflammatory cascade,
promoting antimicrobial peptides (AMPs) (20).
Inflammatory Pathway: AMPs and
Microbiome
As largely examined in multiple skin inflammatory processes,
these mediators, named as defensins (α and β), cathelicidin
(LL37), ribonuclease 7 (RNase7) and psoriasin (S100A7), in light
of the imbalance induced by UVR on keratinocytes and skin
microbiome, have also been investigated in PLE (21, 22). Patra
et al. have found that the expression of psoriasin, RNase7, HBD-2,
and LL-37 was increased in PLE lesional skin, whereas HBD-3
was decreased. Considering the skin surface as a “multiethnic
world,” without forgetting the crucial role of keratinocytes,
we can’t exclude that AMPs release could be determined by
modification in microbiome components after UV interaction
(23). Indeed, microbiome could represent the source, direct or
indirect, of the yet undetected UVR-induced antigens formed in
PLE patients, leading to keratinocyte damage. As a consequence,
LL-37, also induced by UVB, IFNγ, TNF-α, IL-6, could represent
a potential indirect driver of PLE (23). It can form aggregates
with self-nucleic acids able to activate pDCs: in psoriasis it has
been recognized as the main autoantigen (24). Even though in
PLE patients a complete absence of pDCs has been reported
(25), an autoimmune milieu exists, and LL-37 could play a
pivotal role, inducing other inflammatory pathways. In Figure S1
(Supplementary Material), the concepts expressed above are
visualized in a cartoon.
Therapy of Polymorphic Light Eruption:
What’s New?
The first line of treatment for PLE includes sun avoidance,
sunscreens and topical corticosteroids (26). For all patients
preventive management is fundamental during sunny weather,
by avoidance of intense UVR exposure and use of protective
clothing, as well as application of sunscreen, in particular
during the first exposure of the year. New generation broad-
spectrum sunscreens, with high sun protection factor for
UVB (SPF), together with longer wavelength UVA protection,
have been reported to confer total or partial protection
in up to 90% of PLE patients (27, 28). The use of oral
antioxidants and nicotinamide could represent an additional
valid preventive measure for these patients. The beneficial effects
of nicotinamide have been investigated in an uncontrolled
trial of 42 patients, where 60% of them reported complete
abolition of symptoms when taking 2–3 g of nicotinamide
daily, before sun exposure (29). Moreover, an extract of the
tropical fern Polypodiumleucotomos [PL) has been shown to
exert both potent antioxidant and immunomodulatory effects.
Frontiers in Medicine | www.frontiersin.org
Polymorphic Light Eruption: News Overview
When administrated at 480 mg/daily before sun exposure it
significantly reduced skin reactions and subjective symptoms
(30, 31). Regarding topical corticosteroid, even if no trials have
been made to determine their efficacy in PLE, they are widely
used to reduce itch (26). The second line of treatments for
PLE includes systemic corticosteroids and photo(chemo)therapy
(26). In a randomized, double-blind, placebo-controlled trial (32)
the authors suggested the use of 25 mg prednisolone daily for
4–5 days at the onset of the eruption. Although, the potential
long-term side effects of repeated courses of prednisolone
must be considered, it could be advised for patients who
suffer from occasional attacks of PLE, in the absence of any
contraindications. In milder cases of PLE, a self-conditioning
programme by graduate exposure to sunlight in springtime may
be sufficient (33). Whereas, in more severe cases, medically
supervised conditioning/desensitization treatment may be more
appropriate. A course of psoralen and UVA therapy (PUVA),
narrowband (NB)-UVB or broadband (BB)-UVB phototherapy,
usually administered in early spring, can be effective as well
as prophylactic treatment (26). Treatment protocol generally
consists of one course of phototherapy/photochemotherapy over
5–6 weeks. Starting doses depend on minimal erythemal dose
(MED) or minimum phototoxic dose (MPD), and are frequently
50–70% of these measured thresholds with incremental increases.
To maintain the benefit acquired with the desensitizing therapy,
a regular sun exposure throughout summer is advised, otherwise
the hardening could be lost within 4–6 weeks. In the treatment
of PLE, NB-UVB should be preferred to PUVA (strength of
recommendation D; level of evidence 4), because of the lower risk
of photocarcinogenesis, no risk of nausea or other side-effects
associated with the ingestion of MOP, and no need to use post-
treatment eye protection. However, PUVA should be considered,
before other systemic treatments, if NB-UVB has failed or has
previously triggered the eruption. In effect, as described below,
the efficacy has been proved for multiple phototherapy regimens
(BB-UVB, NB-UVB and PUVA), and side-effects, in term of rash
provocation, erythema and itch were found to be more common
with UVB than with PUVA (34). As summarized, in the literature,
the efficacy of PUVA results in a 65–100% photoprotection
rate (34). Multiple comparative studies have been performed,
but from the only randomized controlled trial between PUVA
and NB-UVB plus placebo tablets, three times a week, for 5
weeks, no significant difference in efficacy emerged, considering
occurrence of PLE or outdoor activity restriction (35). In the
10 years retrospective review, reported by Man et al. (36), 170
patients with moderate-to-severe PLE received PUVA and/or
UVB phototherapy. In detail, 8 patients received PUVA, 128
NB-UVB, 5 BB-UVB, and 29 patients, who failed to respond
satisfactorily to NB-UVB, were given PUVA the following year.
Self-assessments were made of the severity, and frequency of
PLE episodes were reported at the follow up visits in autumn
or during the following spring. Good or moderate improvement
was reported in 88% of patients treated with PUVA and in 89%
who received UVB. Of the patients treated with both PUVA
and NB-UVB, the majority preferred PUVA. In another 14-years
retrospective study on 79 patients treated with phototherapy (37),
the efficacy, measured during the following summer in term of
3 September 2018 | Volume 5 | Article 252
Lembo and Raimondo
photoprotection with complete/partial remission, was 65% for
PUVA, 82% for BB-UVB and 83% for UVA alone. In this case
the treatment with PUVA was reserved to more severe PLE
forms.
The mechanisms by which phototherapy induces
photoprotection are not fully understood.
However, in the last years many advances have been
performed. In addition to the well-known effects on
melaninization and epidermal thickening of phototherapy,
a wide range of UV induced immunomodulatory and anti-
inflammatory properties are reported (38). Both UVB and
UVA modulate adhesion molecule expression and induce
soluble mediators, such as a-melanocyte-stimulating hormone,
IL-10 (which suppresses the production of interferon γ) and
prostaglandin E2, that explicate anti-inflammatory actions,
preventing T cells activation and promoting apoptosis of skin
infiltrating T cells (34). Moreover, it has been demonstrated
that prophylactic UV photohardening in PLE patients restores
the UV-induced LC migration from the epidermis to the
skin-draining lymph nodes: one of the key cellular event in
UV-immunosuppression (39). The tolerance induced by LC
is mediated by the release of immunosuppressive cytokine
such as IL-10, and by the interference with maturation and
induction of regulatory T cells (Tregs) (40). Moreover, recently,
an interesting link has been reported among LC, Tregs and
vitamin D3. Indeed, it has been demonstrated that a short-term
1 week topical pre-treatment with the 1,25-dihydroxyvitamin
D analogue, calcipotriol, diminished PLE symptoms after
subsequent experimental photoprovocation (41). In addition, in
a murine study 1,25-dihydroxyvitamin D showed comparable
immunosuppressive effects as UV (42). Another interesting
crosstalk has been highlighted between LCs and mast cells.
In addition to their recognized role in atopy, dermal mast
cells are also responsible for protecting the skin from UVB-
induced inflammation, promoting UV immunosuppression
(40). Human studies have demonstrated that after acute and
chronic UVR exposure, dermal mast cells number increases,
together with the release of IL-10. Overall these data suggest
a potential role for mast cells in PLE, and in the mechanism
of photohardening. In accordance with this, Wolf et al. have
reported, for the first time, that photohardening significantly
increases mast cell density in the papillary dermis of PLE patients
(40). Summarizing, photohardening works in PLE by restoring
the normal UV immune suppressive pathway, involving multiple
cell types. The third line treatment for PLE includes the use
of systemic immunosuppressive drugs, such as azathioprine
and cyclosporine. However, only sporadic cases of patients
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AUTHOR CONTRIBUTIONS
SL projected the manuscript, selected the material for the paper,
wrote the initial draft and corrected the following drafts of the
manuscript. AR was engaged in the writing of the manuscript,
supporting new ideas of contents and style.
SUPPLEMENTARY MATERIAL
The Supplementary Material for this article can be found
online at: https://www.frontiersin.org/articles/10.3389/fmed.
2018.00252/full#supplementary-material
Figure S1 | Interplay between innate and adaptive immune system in a context of
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expressed in keratinocytes of the stratum granulosum and stratum corneum of
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Conflict of Interest Statement: The authors declare that the research was
conducted in the absence of any commercial or financial relationships that could
be construed as a potential conflict of interest.
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